Laryngeal paralysis is a debilitating and sometimes life-threatening clinical problem. The goals of the proposed research are to: 1) assess the treatment effacies for unilateral and bilateral paralysis by measuring changes in voice, airway protection, and respiratory functions in patients following treatment, and 2) develop new dynamic approaches to rehabilitation using functional electrical stimulation (FES) and reinnervation strategies in animal models. Treatments for unilateral paralysis (e.g. teflon injection, thyroplasty) attempt to improve voice quality by medializing the vocal cord. Treatments for bilateral paralysis (e.g. laser arytenoidectomy) aim to enlarge the airway by lateralizing the vocal cord or creating a glottal chink. These approaches are less than ideal, since they improve upon one laryngeal function at the expense of another. They also represent static, irreversible processes that ignore the long term effects of atrophy on vocal cord mass and position. Functional electrical stimulation offers a more physiologic approach to treatment. In case of bilateral paralysis, the paralyzed posterior cricoarytenoid muscles could be stimulated to abduct the vocal cords using inspiratory signals derived from the diaphragm, phrenic nerve, or intrapleural space (abductor pacing). During noninspiratory phases, the vocal cords would passively relax towards the midline, allowing uncompromised voice production and airway protection. In case of unilateral paralysis, a paralyzed adductor or abductor muscle could be stimulated to restore either of these vocal cord functions. Stimulation of a muscle would be triggered by signals derived from its unparalyzed partner on the contralateral side. The ability of electrical stimulation to reanimate the paralyzed larynx will be explored in chronic experiments on canines, implanted with miniaturized stimulation/sensor devices. Studies will also be performed to determine if electrical stimulation can produce other beneficial effects on a denervated laryngeal muscle and the possible course of its reinnervation. Chronic electrical stimulation may prevent or reverse denervation atrophy, and maintain or restore muscle strength to within normal limits. It may make a muscle refractory to reinnervation by a foreign nerve and encourage reinnervation by its own intrinsic nerve. Finally, electrical stimulation in the presence of a d.c. field may attract regenerating nerve fibers that previously innervated the muscle, providing a means for selective reinnervation. Following successful development of an FES approach in animals, experimental studies will begin in patients to compare the treatment efficacy with conventional methods.